OVERALL: ABSTRACT The theme of the Rutgers Center for Environmental Exposures and Disease (CEED) is Precision Environmental Health (PEH) research, which we define as the integration of data from exposure biology, genomics, epigenetics, and microbiomics to identify biological responses that are mechanistically linked to pathogenesis and that will inform disease prevention. The mission of CEED is to improve health and diminish the impact of environmental toxicants and stressors by reducing exposures and mitigating their adverse biological effects. Our vision is that a PEH research approach can better inform the development of precise and targeted prevention/intervention strategies. Our strategy is to recruit and train investigators who can integrate information-rich data streams from new technologies with the Center?s longstanding expertise in clinical, basic, population-based, and community engaged research to reduce the burden of environmental disease, especially in vulnerable and environmental justice communities, which bear the greatest burden of exposures and health disparities. To achieve our strategic vision, CEED is formed as a hub of transdisciplinary research, combining access to cutting-edge technologies and computational approaches with a team of outstanding scientists with expertise in exposure science, mechanistic toxicology, modeling and bioinformatics, human research, epidemiology, and community engagement. CEED aims to reduce adverse health effects of toxicants and stressors through transdisciplinary PEH research that considers all aspects of the individual?s responsiveness that contribute to disease pathogenesis and that uses this information to design mechanistically-guided intervention and prevention strategies. We aim to engage communities and stakeholders in multidirectional interactions and participatory research to: 1) identify exposures that are of concern to communities and have the potential to adversely affect human health; 2) assess and model the extent of exposures in affected populations; 3) identify cofactors (i.e., psychosocial factors, age, sex, genetics, co-morbidity, etc.) and assess their impact on individual responsiveness to toxicants; 4) discover and use biological response indicators that link exposures to mechanisms of disease pathogenesis; 5) develop and implement mechanistically-driven prevention, intervention, and treatment strategies; 6) reduce exposures and mitigate health effects by informing systems changes that alter behaviors, practices, policies and regulations.